Brief return - Collin Brendemuehl is upset that he is so wrong about things...

He had asked a couple of 'wrong' questions about evolution - wondered 'are there' "10 million" random changes were that were required to explain human evolution from a rodent-like ancestor. I explained that the questions did not even make sense. He didn't like that. He 'allowed' that it might only be 1 million. I asked him to name just 1000 of the 'trait changes' he believes exist. Ultimately, he could produce only those listed below, all dealing with the same structure, most of which are likley goverened by but a few genes. After several rounds of Collin trying to change subjects, dodge questions, and accusing me of all manner of things, I told Collin that until he decided to actually address the original issues, I would not allow more of his comments here. He called it 'censorship.'

I left the following reply (I've cleaned up a few typos):

Hilarious hubris...I guess you ignored the parts where I explaiend that the 'parts' you seem to think require their own specific sets of mutations are actually all part of the same structure (a limb, for example) and I provided you a real example of how ALL those things can be affected by a single mutation.In fact, I specifically countered each of your supposed structures and physiological issues, but you bailed.Regarding an arm, you naively believed the following:

1. circulatory system2. bone structure3. muscles4.skin5. foot/hand

Each of these has a variety of qualities that needto change. Let'slista few. There are more, but this is a goodstart.

I provided the example of the FGFR-3 mutation in humans producing dwarfism that affects ALL of those things. ONE SINGLE mutation. I explicitly did not give that as an example of evolution, rather, as an example of how gene changes can ilicit major phenotypic changes.ADDED COMMENT: But then, you insisted that getting a nail from a claw was a "major" phenotypic change requiring many mutations.I explained how several of those 'individual' changes were actuallyessentially the same thing - changing a vessels size will affect it's capacity;making abone larger increases it's "marrow capacity", etc. To noavail.

A rational person might want to quit while they are ahead.

And by the way - even if we are generous and grant that the 20 things you mention are legitimate individual changes each requiring their own suite of mutations (which they are not), YOU said there were MILLIONS, and I asked you to provide 1000.You have 980 more to go. But I suspect that they, too, would all fall under the same umbrella of multiple changes that really are not multiple changes.It is too bad that an untrained internet pseudoexpert cannot realize his limitations and actually acknowledge the possibility that he might not be up to snuff on the things he rants about.Too much to ask, I suppose.And by the way - discretion is not censorship. Post something of substance, and it will get through.

Internet creationist types also seem to like to try to imply - or state outright - that professors and such have some sort of obligation to put up with trollish behavior and address all manner of shallow nonsense presented as unasailable truth. Collin writes:

Now, if the terms I used were too colloquial, the list was certainly subject tocorrection and clarification. A Ph. D. scientist should be able to competentlyaccomplish that.

Um, OK, well, the names were certainly colloquial enough, but that was hardly the issue, as I explained.I can only imagine what he would have written if I had provided the anatomically-correct terms for each of the structures he had referred to - let me guess, I would have been labelled an elitist? I would have been accused of trying to embarrass the poor creationist? I would have been accused of trying to cloud the issues with minutiae?In the end, clarification of terminology is the least of Collin's problems.

10 comments:

Hi Scott,There you go declaring victory again :P. However, my software engineering brain tells me that your argument involving FGFR3 is wrong-headed. It only shows that FGFR3 plays a role in several cellular processes. I could easily change one setting on my computer and it would affect the way all kinds of things look. However, implementing a new feature in a software program generally requires many source code changes in multiple locations. I wonder how many bits of information scattered throughout the human genome besides what’s in FGFR3 affect wound healing.

Randy, Rany, Randy - there you go again, thinking that genomes operate just like software (even though you have admitted before that you recognize that it doesn't... weird...).

It shows that the mutant FGFR-3 alters phenotype during development. It almost certainly alters downstream reactions (affecting other genes' expression) which is likely how it's effects are manifested. But it is the mutation itself that produces the alterations in phenotype.

Which was my point.

Frankly, I don't care what you would do in a software program because genomes are not software. At best, relating genomes to software is a decent introductory analogy, just like langauge analogies are. The problem arises when one takes the analogy too far.

As far as wound healing goes, likely there are many pathways involved. I believe we had discussed that at one point. FGFR-3 probably plays little or no role it wound healing though. Fibroblasts do more than heal wounds.

I understand your point. But I think you would agree that when it comes to mapping sections of DNA to traits there is not a one-to-one mapping. Like software, most mappings would be one-to-many, many-to-one and many-to-many.

Excluding the DNA that you think is junk, how many non-random changes to a chimpanzee genome do you think would be required to transform it into a human genome?

The FGFR3 gene provides instructions for making a protein called fibroblast growth factor receptor 3. This protein is part of a family of fibroblast growth factor receptors that share similar structures and functions. These proteins play a role in several important cellular processes, including regulation of cell growth and division, determination of cell type, formation of blood vessels, wound healing, and embryo development.

The FGFR3 protein spans the cell membrane, so that one end of the protein remains inside the cell and the other end projects from the outer surface of the cell. This positioning of the protein allows it to interact with specific growth factors outside the cell and to receive signals that control growth and development. When these growth factors attach to the FGFR3 protein, the protein triggers a cascade of chemical reactions inside the cell that instruct the cell to undergo certain changes, such as maturing to take on specialized functions.

The FGFR3 protein is involved in the development and maintenance of bone and brain tissue. Researchers believe that this receptor regulates bone growth by limiting the formation of bone from cartilage (a process called ossification), particularly in the long bones.

???

I understand your point. But I think you would agree that when it comes to mapping sections of DNA to traits there is not a one-to-one mapping. Like software, most mappings would be one-to-many, many-to-one and many-to-many.

Indeed, I think I have stated as much in the past.

Excluding the DNA that you think is junk, how many non-random changes to a chimpanzee genome do you think would be required to transform it into a human genome?

None.

It depends on what you mean by non-random, of course. Do you mean non-random as in 'planned' or 'directed', or non-random as in mutations are not actually equally distributed across genomes due to things like poly-purine/pyrimidine stretches, hot spots, etc.?

Suppose you or I had a DNA editor and we could make edits to a chimpanzee genome and transform it into a human genome. Our edits would be non-random because we would know which way to go.

But they would just be copying what had already happened.

So deleting a sequence would be an change. Inserting a sequence would be a change. And moving a sequence would be two changes (a cut and a paste).

How many of those changes would be needed?

No idea.

I would say that it is far fewer than many seem to insist it must be. Creationist electrical engineer Walter ReMine implies that it wopu8ld be more than 500,000 beneficial mutations and 25,000+ expressed neutral changes, for example.

But he is essentially clueless and arguing via big numbers due to the fact that he, like Collin, seems to believe, quite naively, that every single structure or physiologiccal alteration requires a specific suite of beneficial mutations, and there is simply no evidence that that is even remotely the case.

By the way Collin - I haven't looked at your 'response' yet. I am pretty sure it will be a rehash of repeated claims and allegations and a reiteration of the same points, plus the irrelevant addition of some tangential issues.

We'll see how my prediction comes out. I will have some time tomorrow, and maybe I'll take a look at it.